ABSTRACT
Despite breakthroughs in care and treatment, the consequences of a
subarachnoid hemorrhage (SAH) are still associated with morbidity and
mortality. Early brain injury is still a major source of clinical
deterioration in people with SAH.
When a patient suffers a SAH, they are more likely to develop long-term
neurological problems, which can be life-threatening. According to
recent research, the management and remission of SAH are dependent on
inflammatory mechanisms. The development of problems after SAH has
recently been linked to inflammation. Many investigations have failed to
show how inflammatory mechanisms affect SAH patients’ prognosis and
outcome. SAH procedures and management will be improved by better
understanding the various inflammatory pathways that occur after SAH. It
was the goal of this review to outline some of the most important
inflammatory pathways that emerge after SAH and to provide a general
understanding of SAH.
Keywords : inflammation, EBI (early brain injury), cerebral
vasospasm, subarachnoid hemorrhage, secondary brain injury.
INTRODUCTION : Acute subarachnoid hemorrhage (SAH) is a
dangerous illness that affects many organ systems in addition to the
brain (Cardentey-Pereda & Pérez-Falero, 2002).
Subarachnoid hemorrhage (SAH) accounts for around 5% of all strokes
(Hong, Tosun, Kurland, Gerzanich, Schreibman & Simard, 2014), with more
than 30% of patients dying as a result of the first or subsequent
bleeding (Ostrowski, Colohan & Zhang, 2006). Brain injury that occurs
immediately after bleeding is well understood and occurs as a result of
a rise in intracranial pressure and a subsequent fall in cerebral
perfusion. Brain injury that occurs later has a variety of causes and
may necessitate a variety of treatment options because of the different
time windows of varying duration (Schneider, Xu & Vajkoczy, 2018). The
fact that some SAH patients improve while others continue to deteriorate
after their initial spasm is also puzzling (Miller, Turan, Chau &
Pradilla, 2014). Early brain injury (EBI) is primarily responsible for
the poor outcome of subarachnoid hemorrhage (SAH), which is intimately
linked to inflammation (Sun, Duan, Jing, Wang, Hou & Zhang, 2019). In
individuals with subarachnoid hemorrhage (SAH), neuroinflammation is
directly linked to functional prognosis. Microglia are myeloid cells
that make up the CNS’s innate immune system. In response to damage or
disease processes in the CNS, they become highly engaged. The use of
brain injury biomarkers could be useful not only for diagnosing and
identifying intracranial lesions, but also for assessing severity,
prognosis, and therapeutic efficacy (Mrozek, Dumurgier, Citerio, Mebazaa
& Geeraerts, 2014).
SAH-related brain injury has been shown to be protected by inflammation
as a defensive mechanism. In the event of a stroke, blood components
such as red blood cells (RBCs), leukocytes (including macrophages), and
plasma proteins (including Endothelin-1) enter the brain instantly.
There is an inflammatory response as soon as there is blood present in
the parenchyma. Inflammatory cells are mobilized and activated during
this time period. The early inflammatory cells in reaction to the
extravascular blood component are believed to be microglia and
astrocytes.
Inflammatory mechanisms following SAH :
Following SAH, researchers began to look for probable links between
cerebral vasospasm and inflammatory alterations in the CSF, because at
the time, this condition was considered to be the primary, if not the
only, cause of secondary brain injury. SAH-related secondary brain
injury can result from a variety of factors, including traumatic brain
injury (TBI) and SAH. It has been established in both human and animal
research that inflammatory processes can occur in the central nervous
system in conjunction with, contribute to, or even initiate programmed
cell death (Minami, Tani, Maeda, Yamaura & Fukami, 1992). The first
findings on systemic inflammation appeared around the end of the 1990s
and the beginning of the 2000s, and they outlined a peripheral immune
modulation after SAH (Yoshimoto, Tanaka & Hoya, 2001)
Inflammation was merely accounted to occur alongside, or aggravate
cerebral vasospasm, rather than being comprehended as an unique
pathomechanism, when cerebral vasospasm was thought to be the only-or at
least biggest-contributor to subsequent brain injury following SAH
(Schneider, Xu & Vajkoczy, 2018). With more recent studies, it is
believed that not only cerebral vasospasm is a main interest when
talking about secondary brain injury but also, early brain injury is an
important condition. Around this same time, in early 2000, many
mechanisms were studied to show effects of many substances on SAH
(Fassbender et al., 2000).
Although cellular components reach the subarachnoid region from within
the blood arteries, both cellular and molecular factors operate on the
vascular walls, raising the question of whether CSF inflammation is an
outside-in or inside-out event (Schneider, Xu & Vajkoczy, 2018).